L27 Immunology and Skin Flashcards
What are the 3 layers of the skin and the different layers of the topmost layer (top to bottom), and some idea of what cells are in it
Stratum = s.
- Epidermis: keratinocytes
a) s. corneum
b) s. granulosum
c) s.spinosum
d) s. basale: melanocytes
Basement membrane/dermo epidermal junction
- Dermis: CT, bv
- Subcutaneous fat
How does Urticaria present what is happening in the skin, what are potential causes.
Intensely itchy rash (demarcated weals) presenting intermittently <24 hrs on the body.
Can be acute, chronic or anaphylactic
Within the dermis Mast cells are degranulating
Causes
- Physical (pressure, cold, sun, water)
- Infection related
- Immune related (food, drug)
Describe the pathology and treatment of Auto-immune Urticaria (in 30-50% of patients with Chronic urticaria)
Functional IgG antibodies are formed against immunoglobulin IgE attached to mast cells.
Treatment is immunosuppressive
- Ciclosporin (renal SE)
- Omalizumab (binds to IgE in blood and prevents binding of IgE to mast cells)
Compare risk factors for developing Bullous Pemphigoid vs Pemphigus Vulgaris
Risk factors
BP:
-Older patients (70+)
-Cerebrovascular/BBB injury prior to onset due to neural isoform (skin and muscular form also existing) of BP tissue allowing sensitisation for cross reactivity in the skin
PV:
- Younger patients
- Rare
Compare the pathology and therefore presentation of Bullous Pemphigoid vs Pemphigus Vulgaris
BP: autoimmune reaction (igG) against two proteins in the hemi desmosome BP180, 230 which stick the epidermis to dermis
= Leads to itchy rash, then development of full thickness blisters due to separation of epidermis and dermis
PV: autoimmune reaction against desmogleins in the desmosomes that help keratinocytes to stick to each other within the epidermis.
= shallow blisters/skin erosions within the epidermis
What technique is used to differentiate between PV and BP and what are their respective treatments
Direct immunofluorescence
by mixing Anti-human antibodies with a fluorescent tag with skin biopsy.
BP shows staining at the dermo-epidermal junction;
PV shows staining within the epidermis
Treat BP: immunosuppressors eg. Prednisone, azathioprine, methotrexate
Treat PV: Rituximab which binds to b cells and prevents antibody formation + entecavir Hep B release
What are the different types, general presentation and causes of Vasculitis
- Large, med, small depending on vessel
- Can involve Skin, joints, kidneys, GI tract
Skin: small vessel Vasculitis.
- Purpuric rash on likely lower legs. Rash doesn’t blanche as blood leaked out.
- Over time fresh red Hb–> haemosiderin (brown)
Causes for svv
- Immune complex vessel damage by type 3 hypersensitivity reaction potentially caused by chronic Hep B infection
What are the factors that predispose some to atopic dermatitis (eczema) and what does that in turn lead them to greater risk
- Genetic mutation in filaggrin protein which forms a natural moisturiser in the granular layer of epidermis
- The impaired barrier function means that antigens can penetrate the skin easier –>
- Higher prevalence of allergy and contact dermatitis (type 4 hypersensitivity reaction)
Give 3 reasons why patients may be immunosuppressed
- Treating severe disease: eg. BP, PV
- As part of severe disease eg. HIV, severe combined immunodeficiency
- Drugs used required for organ transplantation
How can the culprit of contact dermatitis be found
Patch testing using purified antigens
What are the two complications of Immunosuppression related to skin
Higher susceptibility of
- Infection
- unusually presentation
eg. cutaneous HPV, disseminated Varicella Zoster virus.
- diagnose with skin swab for bacteria/virus, skin biopsy and blood culture. - Neoplasia
- due to suppression of immune surveillance mechanisms to fix UV damage.
- Squamous cell carcinoma, aggressive more likely
- Nicotanimide Vit B3 helps to boost immune system
